By DrQutaiba A Qasim PhD Clinical Biochemistry 2020 Subjects at risk of developing diabetes mellitus 1strong family history of diabetes mellitus 2autoimmune disease 3obesity ID: 1044420
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1. Disorders of CHO metabolim By Dr.Qutaiba A. Qasim Ph.D Clinical Biochemistry2020
2. Subjects at risk of developing diabetes mellitus1-strong family history of diabetes mellitus2-autoimmune disease3-obesity4-sedentary life style5-gestational diabetes6-prediabetes7-Age over 45 years8-stress
3. Metabolic features of diabetes mellitusPatients with type 1 diabetes tend to be diagnosed before the age of 40 years, are usually lean and have experienced weight loss at the time of presentation. They may present with diabetic ketoacidosis. Conversely, patients with type 2 diabetes often present later, usually after the age of 40 years, and are often overweight or obese.
4. Long-term effects of diabetes mellitus1-Macrovascular disease due to abnormalities oflarge vessels may present as coronary artery, cerebrovascular or peripheral vascular insufficiency. The condition is probably related to alterations in lipid metabolism and associated hypertension. The most common cause of death is cardiovascular disease, including myocardial infarction.
5. Long-term effects of diabetes mellitus2-Microvascular disease due to abnormalities of small blood vessels particularly affects the retina (diabetic retinopathy) and the kidney (nephropathy); both may be related to inadequate glucose control.3-Infections4-Diabetic ulcers
6. Monitoring of diabetes mellitus1-Glycosuria 2-Blood glucose3-Glycated haemoglobin (HbA1c) gives a retrospective assessment of the mean plasma glucose concentration during the preceding 6–8 weeks.4-Fructosamine assess glucose control over a shorter time course than that of HbA1c (about 2–4 weeks
7. Monitoring of diabetes mellitus5-Blood ketones6-Urinary albumin
8. Acute metabolic complications of diabetes mellitus1-Hypoglycaemia2-Diabetic ketoacidosis3-Hyperosmolal non-ketotic coma(HONK)4-Lactic acidosis
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10. Principles of treatment of diabetic coma1-Hypoglycaemic coma needs prompt glucose replacement to avoid irreversible brain damage, for example 50 mL of 20 per cent glucose intravenously. If intravenous access is not an option, glucagon 1 mg can be givenintramuscularly. Once the patient is awake, glucose containing drinks can be given.
11. Principles of treatment of diabetic coma2-Diabetic ketoacidosis : Repletion of fluid and electrolytes should be vigorous. A 0.9 per cent normal saline solution should be administered. If the plasma glucose concentration is more than 20 mmol/L, 10 U soluble insulin should be given. If the metabolic acidosis is very severe (pH less than7.0), bicarbonate may be infused .
12. Investigation of suspected diabetes mellitusDiabetes mellitus is confirmed if one of the following is present: a fasting venous plasma concentration of 7.0 mmol/L or more on two occasions or once with symptoms, or a random venous plasma concentration of11.1 mmol/L or more on two occasions or once with symptoms.
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14. HYPOGLYCAEMIAif the plasma glucose concentration is less than 2.5 mmol/L in a specimen collected into a tube containing an inhibitor of glycolysis, for example fluoride oxalate.Bloodcells continue to metabolize glucose in vitro, and lowconcentrations found in a specimen collected withoutsuch an inhibitor can be dangerously misleading(pseudohypoglycaemia).
15. Hyperinsulinaemic hypoglycaemiaInappropriately high insulin concentrations due to:Pancreatic tumour – insulinomaHyperplasia of the pancreatic islet cellsInsulin receptor antibodiesAutoimmune insulin syndromeExogenous insulinSulphonylureas, meglitinides
16. Hypoinsulinaemic hypoglycaemia1-Endocrine : Glucocorticoid deficiency/adrenal insufficiency , Severe hypothyroidism ,Hypopituitarism2-organ failure : Severe liver disease , End-stage renal disease , Severe congestive cardiac failure3-Some non-pancreatic islet cell tumours Insulin-like growth factor (IGF)-2-secreting tumours, e.g. liver, adrenal, breast, Leukaemias, lymphomas
17. Reactive hypoglycaemiaIdiopathicPost-gastric surgeryAlcohol inducedMiscellaneous causesVon Gierke’s disease (type 1 glycogen storage disease)Drugs, e.g. salicylates, quinine, haloperidol,pentamidine, sulphonamides
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20. END OF LECTURETHANKS FOR LISTENING